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Endothelial damage in the presence of pro-inflammatory agents, such as interleukin 1 (IL-1), Tumor Necrosis Factor (TNF), endotoxins, and advanced glycation end-products (AGEs) enhances the expression of adhesion molecules: vascular cell adhesion molecule (VCAM-1), intercellular adhesion molecule (ICAM-1), platelet endothelial cell adhesion molecule (PECAM-1), E-selectin, and P-selectin for leukocyte adhesion [1,5,6]